Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017
Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017
MONDAY, NOVEMBER 27, 2017
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING 63 CASES CONFIRMED TO DATE NOVEMBER 27, 2017
http://chronic-wasting-disease.blogspot.com/2017/11/texas-chronic-wasting-disease-cwd-tse.html
FRIDAY, DECEMBER 01, 2017
TEXAS TAHC CWD TSE PRION SURVEILLANCE AND REPORTING UNDER QUESTION, 14 CAPTIVE CASES CWD DETECTED 2017 SO FAR
http://chronic-wasting-disease.blogspot.com/2017/12/texas-tahc-cwd-tse-prion-surveillance.html
SATURDAY, DECEMBER 02, 2017 TEXAS
TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017
http://chronic-wasting-disease.blogspot.com/2017/12/texas-tahc-cwd-tse-prion-trace-herds.html
WEDNESDAY, OCTOBER 18, 2017
TEXAS Medina County Elk Tests Positive for Chronic Wasting Disease CWD TSE PRION harvested on a high-fenced premises
http://chronic-wasting-disease.blogspot.com/2017/10/texas-medina-county-elk-tests-positive.html
WEDNESDAY, SEPTEMBER 27, 2017
TEXAS, TPWD, WIN CWD COURT CASE AGAINST DEER BREEDERS CAUSE NO. D-1-GN-15-004391
THURSDAY, SEPTEMBER 21, 2017
TEXAS TPWD CWD mandatory check stations for Chronic Wasting Disease in the South Central, Panhandle, and Trans-Pecos areas
WEDNESDAY, MAY 31, 2017
Texas New Exotic CWD Susceptible Species Rules Now in Effect
MONDAY, MAY 15, 2017
TEXAS New CWD TSE PRION 50th Case Discovered at Fifth Captive Deer Breeding Facility
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play
FRIDAY, MARCH 31, 2017
TPWD UPDATE CWD TSE Prion 49 confirmed cases and unwanted firsts for Texas
MONDAY, AUGUST 14, 2017
*** Texas Chronic Wasting Disease CWD TSE Prion History ***
WEDNESDAY, DECEMBER 06, 2017
Arkansas Biological samples reveal 70 new cases of CWD, no new counties affected
WEDNESDAY, AUGUST 16, 2017
ARKANSAS CWD TSE PRION 214 CASES CONFIRMED TO DATE AS OF AUGUST 9, 2017
MONDAY, JUNE 05, 2017
Arkansas CWD Management Zone expands to include Van Buren County 213 cases to date
SUNDAY, MAY 21, 2017
Arkansas Chronic Wasting Disease CWD TSE Prion Roundup 212 Cases Confirmed To Date
TUESDAY, MAY 03, 2016
Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project and Hunkering Down in the BSE Situation Room USDA 1998
http://chronic-wasting-disease.blogspot.com/2016/05/arkansas-chronic-wasting-disease-cwd.html
WEDNESDAY, DECEMBER 13, 2017
WEDNESDAY, DECEMBER 13, 2017
Michigan Chronic Wasting Disease Identified in a Mecosta County Farmed Deer
WEDNESDAY, DECEMBER 06, 2017
Michigan DNR CWD INCREASES TO TOTAL 30 CASES TO DATE
FRIDAY, NOVEMBER 17, 2017
Michigan 11 case CWD confirmed, three additional suspect positives awaiting confirmation
THURSDAY, DECEMBER 07, 2017
Montana Chronic Wasting Disease Found in Deer north of Chester
TUESDAY, DECEMBER 05, 2017
Montana Fish, Wildlife and Parks testing has identified two more cases of chronic wasting disease in Carbon County deer
SATURDAY, NOVEMBER 18, 2017
Madras man cited for failing to follow import restrictions to keep Oregon CWD-free Carcass of first free-ranging Montana deer to test positive for CWD brought to Oregon
TUESDAY, NOVEMBER 14, 2017
Montana Second deer found suspect for CWD
http://chronic-wasting-disease.blogspot.com/2017/11/montana-second-deer-found-suspect-for.html
New York State
CWD has been confirmed in wild and captive deer in NY state back in around 2005. however, they have been either real lucky, or just doing something right (their surveillance system does seem to be a bit better than others), because cwd has not been detected there in some time, around a decade or so, if my mind does not fail me...i don't recall the total figures, 5 or so captive and 3 or so in the wild in 2005. ...quick look at files;
WEDNESDAY, NOVEMBER 08, 2017
Montana CWD sample comes back suspect, second sample submitted
WEDNESDAY, NOVEMBER 08, 2017
Montana Chronic Wasting Disease CWD TSE Prion Response Plan Singeltary Submission
New York State Chronic Wasting Disease CWD TSE Prion History in Wild and Capitve Herds
New York State
CWD has been confirmed in wild and captive deer in NY state back in around 2005. however, they have been either real lucky, or just doing something right (their surveillance system does seem to be a bit better than others), because cwd has not been detected there in some time, around a decade or so, if my mind does not fail me...i don't recall the total figures, 5 or so captive and 3 or so in the wild in 2005. ...quick look at files;
New York State Chronic Wasting Disease CWD TSE Prion History in Wild and Capitve Herds
Subject: POSITIVE CASE OF CWD FOUND IN ONEIDA COUNTY NY DEER
From: "Terry S. Singeltary Sr." <flounder@WT.NET>
Reply-To: Bovine Spongiform Encephalopathy L@KALIV.UNI
Date: Thu, 31 Mar 2005 13:50:50 -0600
Content-Type: text/plain Parts/Attachments: Parts/Attachments text/plain (107 lines) Reply Reply
##################### Bovine Spongiform Encephalopathy #####################
Department of Agriculture & Markets News Thursday, March 31, 2005 Contact: Jessica A. Chittenden 518-457-3136 jessica.chittenden@agmkt.state.ny.us
------------------------------------------------------------------------
POSITIVE CASE OF CWD FOUND IN ONEIDA COUNTY DEER Mandatory Testing Protocols Find CWD in a Captive White-Tailed Doe
The first positive case of chronic wasting disease (CWD) in New York State has been confirmed in a white-tailed doe from a captive herd in Oneida County. CWD is a transmissible disease that affects the brain and central nervous system of deer and elk.
There is no evidence that CWD is linked to disease in humans or domestic livestock other than deer and elk.
The animal that tested positive for CWD was a six-year old white-tailed doe that was slaughtered from a captive herd in Oneida County as part of the State s mandatory CWD surveillance and testing protocols. Preliminary tests performed at the New York State Veterinary Diagnostic Laboratory at Cornell University determined the presumptive positive, which was confirmed late yesterday by the National Veterinary Services Laboratory in Ames, Iowa.
The New York State Department of Agriculture and Markets has officially quarantined the index herd in which the positive deer was found, and will depopulate and test all deer on the premises. Other herds associated with the index herd have also been quarantined and an investigation has been initiated to find and test any susceptible deer that came into contact with the index herd and to assess the health and environmental risks associated with such establishments. The Department of Environmental Conservation (DEC) will conduct intensive monitoring of the wild deer population surrounding the index herd to ensure CWD has not spread to wild deer.
CWD is a transmissible spongiform encephalopathy (TSE) of deer and elk. Scientific and epidemiological research into CWD is ongoing. To date, research shows that the disease is typified by chronic weight loss, is always fatal, and is transmissible between susceptible species. CWD has only been found in members of the deer family in North America, which include white-tailed deer, mule deer, elk and moose.
CWD has been detected in both wild and captive deer and elk populations in isolated regions of North America. To date, CWD has been found in Colorado, Illinois, Kansas, Minnesota, Montana, Nebraska, New Mexico, Oklahoma, South Dakota, Utah, Wisconsin and Wyoming in the United States, and in Saskatchewan and Alberta in Canada.
Establishing the known CWD health status of captive and wild cervid populations is a critical component for controlling CWD. In New York, the responsibility for controlling CWD is shared between the State Department of Agriculture and Markets, DEC, and the U.S. Department of Agriculture s (USDA) Animal and Plant Health Inspection Service (APHIS). New York s cooperative, active surveillance program serves as a model for the nation in CWD control.
The State Department of Agriculture and Markets monitors the health and movement of all captive deer and elk for the presence of common livestock diseases, including CWD. In July 2004, the Department initiated the CWD Enhanced Surveillance and Monitoring Program, which requires captive deer and elk herd owners to take various actions, including routine sampling and testing, animal identification and an annual herd inventory. Since the inception of testing for CWD in 2000, 681 captive deer and elk have been tested and found negative for CWD.
DEC issues licenses to individuals who possess, import or sell white-tailed deer. DEC also routinely tests New York s wild deer population. Following the discovery of CWD in Wisconsin, DEC implemented a statewide surveillance program in April 2002 to test wild white-tailed deer for the presence of CWD. Samples are collected and sent to an approved USDA laboratory for analysis. To date, DEC has taken samples from 3,457 wild white-tailed deer, including 40 from the county where the positive deer was found. All samples from wild white-tailed deer have tested to date have been negative for CWD.
DEC will also implement precautionary regulations limiting transportation and possession of whole carcasses and some parts of wild deer taken near the location of the captive herd. These regulations will be similar to those currently in place for importation of carcasses and parts of deer into New York.
DEC has also implemented regulations restricting various activities to help control CWD within the State, including restrictions on the importation of live deer and elk, deer feeding, importation and possession of certain deer parts and carcasses, and transportation of deer and elk carcasses through New York State.
USDA APHIS supports individual State programs by providing funding for CWD prevention and surveillance. USDA APHIS reimburses states conducting CWD testing on their wild and captive cervid population and also provides indemnification dollars for captive herds that must be destroyed due to the presence of CWD.
New York State has 433 establishments raising 9,600 deer and elk in captivity. In the wild, DEC estimates there are approximately one million deer statewide.
###
TSS
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
Re: CHRONIC WASTING DISEASE FOUND IN ONEIDA COUNTY WILD DEER
Terry S. Singeltary Sr. <flounder@WT.NET> Thu, 28 Apr 2005 20:49:23 -0500 429 lines
CHRONIC WASTING DISEASE FOUND IN ONEIDA COUNTY WILD DEER
The New York State Department of Environmental Conservation (DEC) today announced it has received a preliminary positive result for chronic wasting disease (CWD) in a wild deer sampled in Oneida County. If confirmed, this will be the first known occurrence of CWD in the wild in New York State.Terry S. Singeltary Sr. <flounder@WT.NET> Thu, 28 Apr 2005 09:13:20 -0500 145 lines
DEC TO TEST FOR CHRONIC WASTING DISEASE IN HAMILTON COUNTY Terry S. Singeltary Sr. <flounder@WT.NET> Thu, 14 Apr 2005 16:26:38 -0500 95 lines
CWD NY CONSUMPTION AND CONTACT 'DON'T TOUCH THAT ANIMAL' or 'don't worry, be happy'
Terry S. Singeltary Sr. <flounder@WT.NET> Sat, 9 Apr 2005 11:30:23 -0500 111 lines New Thread
CWD NY DEPT OF HEALTH FACTS AND FICTION CWD NY DEPT OF HEALTH FACTS AND FICTION
Terry S. Singeltary Sr. <flounder@WT.NET> Sun, 10 Apr 2005 14:44:06 -0500 1827 lines
CWD UPDATE, TEST RESULTS REVEAL ***THREE ADDITIONAL POSITIVES FROM INDEX HERD
Terry S. Singeltary Sr. <flounder@WT.NET> Fri, 8 Apr 2005 17:07:46 -0500 97 lines
DEC RELEASES RESULTS OF TESTS FOR CHRONIC WASTING DISEASE Oneida County to Date Shows No Signs of CWD in Wild Herd
DEC has implemented intensive monitoring efforts after CWD was found in two captive white-tailed deer herds in Oneida County – the first incidents of CWD in New York State.
***Earlier this month, the State Department of Agriculture and Markets (DAM) completed testing of the captive deer and found a total of
***five positive results for CWD in the two captive herds.
Terry S. Singeltary Sr. <flounder@WT.NET>
CHRONIC WASTING DISEASE UPDATE NEW YORK Herds Depopulated, Public Meeting Scheduled for Friday
Terry S. Singeltary Sr. <flounder@WT.NET> Wed, 6 Apr 2005 15:59:50 -0500 115 lines
you can see a run down on cwd in NY state here;
SUNDAY, DECEMBER 03, 2017
Ohio Chronic Wasting Disease Update Through November 2017
WEDNESDAY, NOVEMBER 15, 2017
Ohio ODNR Continues Plan to Monitor Ohio’s Deer Herd for Chronic Wasting Disease or do they?
WEDNESDAY, AUGUST 16, 2017
OHIO Chronic Wasting Disease CWD TSE Prion UPDATE?
Ohio Deer Hunting Season 2017-2018 Today, the deer population in Ohio exceeds 750,000.
see map;
WEDNESDAY, AUGUST 05, 2015
Ohio confirms to me Chronic Wasting Disease
CWD Spreads 19 confirmed cases to date Just got off the phone with Christy Clevenger of Ohio
Ohio Department of Agriculture March 2012 – Present (3 years 6 months) Reynoldsburg, Ohio CWD program
Ms. Clevenger confirmed, to date, from the Yoder debacle, 1 confirmed case of CWD from the Hunting Preserve, 2 confirmed cases from the Breeding Farm, and 16 confirmed cases of CWD from the Breeder Depopulation, with a total to date of 19 cases of CWD in Ohio...with sad regards, Terry
http://chronic-wasting-disease.blogspot.com/2015/08/ohio-confirms-to-me-chronic-wasting.html
FRIDAY, DECEMBER 15, 2017
Pennsylvania Four Deer Test Positive for Chronic Wasting Disease on Franklin, Fulton County Quarantined Hunting Preserves
THURSDAY, SEPTEMBER 28, 2017
Pennsylvania GAME COMMISSION OFFERS FREE CWD TESTS FOR DMA-HARVESTED DEER
THURSDAY, SEPTEMBER 21, 2017
Pennsylvania Game Commission has scheduled a series of public meetings to ensure Pennsylvanians remain informed about chronic wasting disease CWD TSE Prion
SATURDAY, AUGUST 12, 2017
*** Pennsylvania 27 deer from Bedford County farm test positive for chronic wasting disease ***
WEDNESDAY, JULY 12, 2017
PENNSYLVANIA CWD FOUND IN THE WILD IN CLEARFIELD COUNTY
THURSDAY, JUNE 01, 2017
PENNSYLVANIA Third Case of CWD Discovered in a Captive Deer Farm in Four Months
MONDAY, MAY 15, 2017
Pennsylvania 25 more deer test positive for CWD TSE PRION in the wild
WEDNESDAY, MARCH 01, 2017
South central Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease
FRIDAY, JANUARY 13, 2017
Pennsylvania Deer Tests Positive for Chronic Wasting Disease four-year-old white-tailed deer Franklin County Hunting Preserve
Wednesday, May 11, 2016
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL CONTROL MEASURES
TUESDAY, NOVEMBER 28, 2017
South Carolina Chronic Wasting Disease CWD TSE Prion Emergency Response Plan?
> Over the past five years, samples collected using this approach resulted in over 1,500 deer testing negative for CWD.
> Surveillance since 2002 has included samples from all 46 South Carolina counties and over 6,000 total deer have been tested.
SO, to put this in perspective, in South Carolina, anywhere from 750,000 to 1,000,000 deer in South Carolina in any give year, and from that, in the past five years, only 1,500 deer tested for CWD tse prion, and from the year 2002, around 15 years, only 6,000 deer have been tested for CWD tse prion in South Carolina. That is not enough CWD testing folks, for anyone wanting to find CWD TSE Prion. IF you wait for CWD to find you, you have failed terribly, because it will find you, but by then it's much too late. If you think game farms are the only culprits helping to introduce CWD into your state, you are only fooling yourselves. you can't wish cwd away, you can't hope it will not find you, because it will, ask Norway, CWD knows no borders, National or International.
Now, a few concerning aspects of the statements by SCDNR et al,
Can CWD infect livestock or other wildlife?
There is no evidence that CWD can be naturally transmitted to livestock or other (non-deer) animals. Susceptibility of exotic deer species (e.g., fallow deer, reindeer, muntjac, etc.) remains unknown.
Is CWD dangerous to humans?
The World Health Organization (WHO) and the federal Centers for Disease Control and Prevention (CDC) have conducted investigations for any relationships between CWD and human neurological disease. These organizations state that there currently is no scientific evidence that CWD has infected humans. However, public health officials recommend that human exposure to the CWD agent be avoided as they continue to evaluate the potential risk, if any.
NOW, let's review the updated peer review science from PRION 2017 2016 2015 CONFERENCEs, and transmission studies, shall we. we will review humans first, and then other animals, and risk factors for Chronic Wasting Disease CWD TSE Prion in Cervid.
THURSDAY, DECEMBER 14, 2017
Governor Scott Walkers Apathy Condemns Wisconsin to a lifetime of Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease
SATURDAY, NOVEMBER 11, 2017
Wisconsin Confirmation of chronic wasting disease CWD two white-tailed deer hunting ranch Waupaca County another farm in Iowa County being quarantined
TUESDAY, OCTOBER 31, 2017
Wisconsin Chronic Wasting Disease CWD TSE Prion Update
TUESDAY, OCTOBER 03, 2017
Wisconsin CWD-positive white-tailed deer found on Shawano County hunting ranch
SUNDAY, OCTOBER 01, 2017
WISCONSIN CHRONIC WASTING DISEASE CWD SAMPLING UPDATE
THURSDAY, AUGUST 03, 2017
Wisconsin CWD Showing Up in Northern Wisconsin Deer Farms
MONDAY, MARCH 20, 2017
Wisconsin CWD TSE Prion Annual Roundup 441 positive
WEDNESDAY, NOVEMBER 15, 2017
Wyoming Game and Fish Department diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 118 near Meeteetse
SATURDAY, OCTOBER 21, 2017
Endemic chronic wasting disease causes mule deer population decline in Wyoming
WEDNESDAY, JULY 26, 2017
Wyoming CWD found in new elk hunt area in Southeast Washakie County CWD found in new elk hunt area in Southeast Washakie County
MONDAY, MARCH 27, 2017
Wyoming CWD Postive Mule Deer Doe Near Pinedale
WEDNESDAY, MARCH 01, 2017
Wyoming mule deer test positive for CWD in Cody
WEDNESDAY, JULY 26, 2017
Chronic wasting disease continues to spread Disease of cervids causing local population declines
NORWAY CHRONIC WASTING DISEASE CWD TSE PRION
TUESDAY, DECEMBER 05, 2017
Norway 30,000 deer animals have so far been tested for Skrantesyke chronic wasting disease CWD TSE PRION DISEASE
THURSDAY, NOVEMBER 30, 2017
Norway Animal welfare surveillance at Nordfjella Skrantesjuke CWD TSE Prion Update
WEDNESDAY, NOVEMBER 29, 2017
Norway another case of Skrantesjuke CWD TSE Prion Adult Reindeer pitcher field in Nordfjella (preliminary testing) 13th case if confirmed
FRIDAY, NOVEMBER 24, 2017
Norwegian Food Safety Authority makes changes to measures to limit the spread of disease Skrantesjuke (CWD) in deer wildlife
SATURDAY, NOVEMBER 18, 2017
Norway detects more Chronic Wasting Disease CWD TSE Prion Skrantesjuke
This is the eighth case of the lethal deer disease in the area since the survey started in 2016.
The reindeer cub was shot by a flock from the Norwegian National Guard, and the infectious agent was detected in the animal's lymph nodes.
WEDNESDAY, NOVEMBER 01, 2017
Norway detects CWD Skrantesjuke Deer possibly atypical Nor-98-type TSE?
Greetings TSE prion world,
i am seeing more and more references to the atypical Nor-98-type CWD TSE Prion in Norway as being of the non-infectious or non-infective variant. with science documented to date, i do not believe that any CWD Skrantesjuke TSE Prion typical or atypical in Norway or anywhere else can be classified as ''non-infective variant''. IF, Norway takes the USDA OIE views and makes atypical Nor-98 type CWD in Deer a International trading commodity fueled by junk science, as they did with sheep, i.e. no trade restrictions for Nor-98 in sheep, the world should then weep...terry
Nor-98 atypical Scrapie Transmission Studies Review
snip...see full text;
FRIDAY, OCTOBER 13, 2017
Norway, Two More New Cases of Chronic Wasting Disease CWD TSE Prion Skrantesjuke
TUESDAY, OCTOBER 10, 2017
Norway detects another case of CWD TSE PRION Skrantesjuke
SATURDAY, SEPTEMBER 30, 2017
Norway, CWD TSE Prion, Humans, Zoonosis, Fortsatt lite sannsynlig at mennesker kan smittes av skrantesyke?
MONDAY, AUGUST 14, 2017
NORWAY CWD, SHEEP GRAZING, and Scrapie, What If?
TUESDAY, JUNE 20, 2017
Norway Confirms 6th Case of Skrantesjuke CWD TSE Prion Disease
Tuesday, December 13, 2016
Norway Chronic Wasting Disease CWD TSE Prion disease Skrantesjuke December 2016 Update
Thursday, September 22, 2016
NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION Skrantesjuke
Saturday, September 03, 2016
NORWAY Regulation concerning temporary measures to reduce the spread of Chronic Wasting Disease (CWD) as 4th case of skrantesjuke confirmed in Sogn og Fjordane
Wednesday, August 31, 2016
*** NORWAY CONFIRMS 4TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN SECOND CARIBOU
Wednesday, August 31, 2016
NORWAY CONFIRMS 4TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN SECOND CARIBOU
Tuesday, August 02, 2016
Chronic wasting disease of deer – is the battle to keep Europe free already lost?
Tuesday, June 14, 2016
*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag Norway ***
Thursday, July 07, 2016
Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd Norwegian moose
14/06/2016 - Norway reports a third case
Tuesday, April 12, 2016
The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging reindeer from the Nordfjella population in South-Norway.
Saturday, April 9, 2016
The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer (Rangifer tarandus tarandus)
Department for Environment, Food and Rural Affairs
Saturday, July 16, 2016
Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy) The British Deer Society 07/04/2016
Red Deer Ataxia or Chronic Wasting Disease CWD TSE PRION?
could this have been cwd in the UK back in 1970’S ???
Clinical Communication Enzootic ataxia in Red deer
P.R. Wilson , Marjorie B. Orr & E.L. Key Pages 252-254 | Published online: 23 Feb 2011
SEE FULL TEXT ;
SATURDAY, JANUARY 14, 2017
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017 ***
SUNDAY, JULY 17, 2016
*** CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016 ***
Saturday, December 12, 2015
*** CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
P178 Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
Dr Laura Pirisinu1, Dr Linh Tran2, Dr Gordon Mitchell3, Dr Aru Balachandran3, Dr Thierry Baron4, Dr Cristina Casalone5, Dr Michele Di Bari1, Dr Umberto Agrimi1, Dr Romolo Nonno1, Dr Sylvie Benestad2 1Department of Veterinary Public Health and Food Safety, Istituto Superiore di Sanità, Rome, Italy, 2Norwegian Veterinary Institute, Oslo, Norway, 3Canadian Food Inspection Agency, National and OIE Reference Laboratory for Scrapie and CWD, Ottawa Laboratory Fallowfield, Ottawa, Canada, 4Neurodegenerative Diseases Unit, ANSES - French Agency for Food, Environmental and Occupational Health & Safety, Lyon, France, 5Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Turin, Italy
Aims: In 2016, Chronic Wasting Disease (CWD) was detected for the first time in Europe in three wild Norwegian reindeer (Rangifer tarandus tarandus) and in two moose (Alces alces). The biochemical analysis and the immunohistochemical distribution of PrPSc from Norwegian reindeer revealed a pattern similar to North American (NA) isolates¹. In this study, we studied the biochemical features of PrPSc from the two CWD cases in Norwegian moose.
Methods: Western blot (WB) analysis of PK-treated PrPSc (PrPres) from Norwegian moose and reindeer isolates was performed according to the ISS discriminatory WB protocol (used in BSE and scrapie Italian surveillance). PrPres fragments were determined by epitope mapping (SAF84, L42, 9A2, 12B2 mAbs), before and after deglycosylation. CWD isolates from Canadian cervids (wapiti, moose and white tailed deer) and a panel of small ruminant and bovine prion strains circulating in Europe were also analysed.
Results: WB analysis with different mAbs showed that PrPres from both Norwegian moose samples was different from that usually associated with CWD in cervids. Indeed, their main C-terminal fragment had a MW lower than the other CWD isolates, and could be discriminated by the absence of the 12B2 epitope. Furthermore, while NA CWD PrPSc is composed of a single PrPres fragment, Norwegian moose samples had an additional C-terminal PrPres fragment of ~13 kDa (CTF13). Among ovine TSEs, classical scrapie and Nor98 were discriminated from both Norwegian moose isolates, while CH1641 samples had molecular features partially overlapping with the moose, i.e. a low MW PrPres and the presence of CTF13. In contrast, moose PrPSc did not overlap with any bovine PrPSc. Indeed, the MW of moose PrPres was lower than H-BSE and similar to C-BSE and L-BSE PrPres, but the two bovine prions lacked additional PrPres fragments.
Conclusions: Unexpectedly, PrPSc from Norwegian moose revealed features substantially different from all other CWD isolates. The PrPSc pattern of Norwegian moose was also different from Canadian moose, suggesting that the variant PrPSc type observed does not simply reflect a host factor and could represent a new CWD strain. Furthermore, PrPSc of Norwegian moose can be easily discriminated from all BSE types, classical scrapie and Nor98, while showing significant overlapping only with CH1641.
Bioassay in voles will help to clarify whether the different PrPSc types observed reflect the presence of a new CWD strain in Norwegian moose, and its relationships with known animal TSEs.
References:
¹Benestad et al. Vet Res (2016)47:88
=====PRION2017====
CH1641 atypical scrapie or atypical BSE or both ???
P178 Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
Dr Laura Pirisinu1, Dr Linh Tran2, Dr Gordon Mitchell3, Dr Aru Balachandran3, Dr Thierry Baron4, Dr Cristina Casalone5, Dr Michele Di Bari1, Dr Umberto Agrimi1. Dr Romolo Nonno1, Dr Sylvie Benestad2
1Department of Veterinary Public Health and Food Safety, Istituto Superiore di Sanita, Rome, Italy, 2Norwegian Veterinary Institute, Oslo, Norway, 3Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD, Ottawa Laboratory Fallowfield, Ottawa, Canada, 4Neurodeqenerative Diseases Unit, ANSES - French Agency for Food, Environmental and Occupational Health & Safety, Lyon, France, 5Istituto Zooprofilattico Sperimentale del Pietnonte, Liguria e Valle d'Aosta, Turin, Italy
Aims: In 2016, Chronic Wasting Disease (CWD) was detected for the first time in Europe in three wild Norwegian reindeer (Rangifer tarandus tarandus) and in two moose (Alces alces). The biochemical analysis and the immunohistochemical distribution of PrPSc from Norwegian reindeer revealed a pattern similar to North American (NA) isolates1. In this study, we studied the biochemical features of PrPSc from the two CWD cases in Norwegian moose.
Methods: Western blot (WB) analysis of PK-treated PrPSc (PrPres) from Norwegian moose and reindeer isolates was performed according to the ISS discriminatory WB protocol (used in BSE and scrapie Italian surveillance). PrPres fragments were determined by epitope mapping (SAF84, L42, 9A2, 12B2 mAbs), before and after deglycosylation. CWD isolates from Canadian cervids (wapiti, moose and white tailed deer) and a panel of small ruminant and bovine prion strains circulating in Europe were also analysed.
Results: WB analysis with different mAbs showed that PrPres from both Norwegian moose samples was different from that usually associated with CWD in cervids. Indeed, their main C-terminal fragment had a MW lower than the other CWD isolates, and could be discriminated by the absence of the 12B2 epitope. Furthermore, while NA CWD PrPSc is composed of a single PrPres fragment, Norwegian moose samples had an additional C-terminal PrPres fragment of ~13 kDa (CTF13). Among ovine TSEs, classical scrapie and Nor98 were discriminated from both Norwegian moose isolates, while CH1641 samples had molecular features partially overlapping with the moose, i.e. a low MW PrPres and the presence of CTF13. In contrast, moose PrPSc did not overlap with any bovine PrPSc. Indeed, the MW of moose PrPres was lower than H-BSE and similar to C-BSE and L-BSE PrPres, but the two bovine prions lacked additional PrPres fragments.
Conclusions: Unexpectedly, PrPSc from Norwegian moose revealed features substantially different from all other CWD isolates. The PrPSc pattern of Norwegian moose was also different from Canadian moose, suggesting that the variant PrPSc type observed does not simply reflect a host factor and could represent a new CWD strain. Furthermore, PrPSc of Norwegian moose can be easily discriminated from all BSE types, classical scrapie and Nor98, while showing significant overlapping only with CH1641. Bioassay in voles will help to clarify whether the different PrPSc types observed reflect the presence of a new CWD strain in Norwegian moose, and its relationships with known animal TSEs.
References: 1Benestad et al, Vet Res (2016}47:88
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
please see;
***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.
***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice
Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2
1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO
Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.
Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.
Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.
Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
WS-02
Scrapie in swine: A diagnostic challenge
Justin J Greenlee1, Robert A Kunkle1, Jodi D Smith1, Heather W. Greenlee2
1National Animal Disease Center, US Dept. of Agriculture, Agricultural Research Service, United States; 2Iowa State University College of Veterinary Medicine
A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested.
Since swine can be fed rations containing ruminant derived components in the United States and many other countries, we conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the brains of clinically ill sheep from the 4th passage of a serial passage study of the U.S scrapie agent (No. 13-7) through susceptible sheep that were homozygous ARQ at prion protein residues 136, 154, and 171, respectively. Pigs were inoculated intracranially (n=19) with a single 0.75 ml dose or orally (n=24) with 15 ml repeated on 4 consecutive days. Necropsies were done on a subset of animals at approximately six months post inoculation (PI), at the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of TSE until study termination at 80 months PI or when removed due to intercurrent disease (primarily lameness). Brain samples were examined by immunohistochemistry (IHC), western blot (WB), and enzyme-linked immunosorbent assay (ELISA). Brain tissue from a subset of pigs in each inoculation group was used for bioassay in mice expressing porcine PRNP.
At six-months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more methods: IHC (n=4), WB (n=3), or ELISA (n=5). Interestingly, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study).
Swine inoculated with the agent of scrapie by the intracranial and oral routes do not accumulate abnormal prion protein (PrPSc) to a level detectable by IHC or WB by the time they reach typical market age and weight. However, strong support for the fact that swine are potential hosts for the agent of scrapie comes from positive bioassay from both intracranially and orally inoculated pigs and multiple diagnostic methods demonstrating abnormal prion protein in intracranially inoculated pigs with long incubation times.
Curriculum Vitae
Dr. Greenlee is Research Veterinary Medical Officer in the Virus and Prion Research Unit at the National Animal Disease Center, US Department of Agriculture, Agricultural Research Service. He applies his specialty in veterinary anatomic pathology to focused research on the intra- and interspecies transmission of prion diseases in livestock and the development of antemortem diagnostic assays for prion diseases. In addition, knockout and transgenic mouse models are used to complement ongoing experiments in livestock species. Dr. Greenlee has publications in a number of topic areas including prion agent decontamination, effects of PRNP genotype on susceptibility to the agent of sheep scrapie, characterization of US scrapie strains, transmission of chronic wasting disease to cervids and cattle, features of H-BSE associated with the E211 K polymorphism, and the development of retinal assessment for antemortem screening for prion diseases in sheep and cattle. Dr. Greenlee obtained his DVM degree and completed the PhD/residency program in Veterinary Pathology at Iowa State University. He is a Diplomate of the American College of Veterinary Pathologists.
RESEARCH ARTICLE
Phenotype Shift from Atypical Scrapie to CH1641 following Experimental Transmission in Sheep
Marion M. Simmons*, S. Jo Moore¤a , Richard Lockey¤b , Melanie J. Chaplin, Timm Konold, Christopher Vickery, John Spiropoulos Animal and Plant Health Agency—Weybridge, Woodham Lane, Addlestone, Surrey, KT15 3NB, United Kingdom ¤a Current address: School of Veterinary and Biomedical Sciences, Murdoch University, South Street, Murdoch, Western Australia, 6150, Australia ¤b Current address: University of Southampton, Southampton, SO17 1BJ, United Kingdom * marion.simmons@apha.gsi.gov.uk
Abstract
The interactions of host and infecting strain in ovine transmissible spongiform encephalopathies are known to be complex, and have a profound effect on the resulting phenotype of disease. In contrast to classical scrapie, the pathology in naturally-occurring cases of atypical scrapie appears more consistent, regardless of genotype, and is preserved on transmission within sheep homologous for the prion protein (PRNP) gene. However, the stability of transmissible spongiform encephalopathy phenotypes on passage across and within species is not absolute, and there are reports in the literature where experimental transmissions of particular isolates have resulted in a phenotype consistent with a different strain. In this study, intracerebral inoculation of atypical scrapie between two genotypes both associated with susceptibility to atypical forms of disease resulted in one sheep displaying an altered phenotype with clinical, pathological, biochemical and murine bioassay characteristics all consistent with the classical scrapie strain CH1641, and distinct from the atypical scrapie donor, while the second sheep did not succumb to challenge. One of two sheep orally challenged with the same inoculum developed atypical scrapie indistinguishable from the donor. This study adds to the range of transmissible spongiform encephalopathy phenotype changes that have been reported following various different experimental donor-recipient combinations. While these circumstances may not arise through natural exposure to disease in the field, there is the potential for iatrogenic exposure should current disease surveillance and feed controls be relaxed. Future sheep to sheep transmission of atypical scrapie might lead to instances of disease with an alternative phenotype and onward transmission potential which may have adverse implications for both public health and animal disease control policies.
snip...
Discussion
It is clear from all the different aspects of phenotype investigated in this study that one recipient sheep in this experimental transmission expressed a phenotype that was CH1641-like, and different from that of the donor which was diagnosed with atypical scrapie. At present this is a single event, and no conclusion can be drawn about the frequency with which this might happen either experimentally or in the field. With only two animals challenged intracerebrally, and the other recipient remaining negative, it will be impossible to extrapolate whether our finding is truly a stochastic single event, or whether a larger group size would have revealed a trend. The very small group size was an inevitable consequence of the practical limitations of this study given the decision to use only naturally-occurring field case donors, for which material is often sparse and frequently of very poor quality. However, this study provides evidence for the view that conversion/mutation of TSE strains is possible and, irrespective of whether or not such events are stochastic, they can lead to the emergence of potentially zoonotic strains.
There are a number of hypothetical explanations for this unexpected result. The first possibility that had to be excluded was that cross contamination with a CH1641 isolate might have occurred at some point in the experimental procedure. The inoculum was prepared and divided into aliquots on the day of preparation; sheep and mice were challenged using different aliquots of the same homogenate. The only strain identified in mice was atypical scrapie, which was compatible with the diagnosis in the original donor. In addition CH1641 had only been handled by the inoculum preparation team once, two years prior to the inocula for this experiment being prepared, arguing against cross contamination during the preparation of the inoculum. Therefore any possible cross contamination would have had to occur during the inoculation procedure. However, on the inoculation day no CH1641 was handled in the operating theatre—only atypical scrapie, and sterile disposable surgical equipment was used wherever possible and reusable equipment was decontaminated according to strict criteria (one hour immersion in 2M NaOH, followed by autoclaving for 18 mins at 136°C). Additionally, an audit of all prepared CH1641 samples indicated that all the anticipated samples remain in our archive and could not, therefore, have been used in error.
Another possible hypothesis is that the donor sheep might have been co-infected sub-clinically with a CH1641-like classical scrapie strain in addition to atypical scrapie. Such co-infection of different scrapie strains, while observed very rarely, has already been described in field situations [23,37], and in the laboratory context, there is supporting evidence for some heterogeneity of strain populations [38] which may then propagate differently in different hosts.
Since the donor animal was an ARR/ARR genotype, this would further reduce the likelihood of a classical scrapie strain co-existing in this sheep, since there are only two confirmed cases of classical scrapie occurring naturally in this genotype [39]. Alternatively, it could be argued that a resistant sheep could potentially be more likely to harbour low levels of a classical scrapie strain which could remain below detection levels of the currently available laboratory tests, given that little is understood about the fundamental basis for genetic resistance. However, surveillance records were reviewed for details relating to the source flock, and there has been no recorded occurrence of classical scrapie in any genotype of animal from this flock, at any time.
The third, and arguably the most plausible, explanation is that the original atypical isolate has ‘converted/mutated’ into CH1641 as a result of the experimental conditions. Again there is some precedent for this occurrence, with previous experimental observations in porcine transgenic mice, where an atypical scrapie isolate acquired a typical 3-band blot pattern with characteristics similar to sub-passaged ovine BSE [40]. This example relates to a cross-species transmission, but evidence also exists of a bovine isolate ‘converting’ or splitting in PRNP congenic TgBov mice [26]. If this was to occur in the field it could be speculated that a country such as Portugal, in which, for several years, atypical scrapie was reported in the absence of any classical scrapie, would be a good place to look for evidence of this kind of strain conversion. However, none of the few recently reported classical scrapie cases in Portugal were CH1641- like [41]. Under natural conditions, and assuming that the atypical scrapie agent is shed into the environment at all, animals are most likely exposed to only very small quantities of the agent, over a prolonged period of time, and probably by the oral route. In contrast, in the current study, a significant amount of the agent was inoculated directly to the brain thereby bypassing all potential natural physiological barriers to the disease. This may have put a greater pressure on the agent to propagate and evolve leading to the observed strain conversion. The difference of genotype between donor and recipient sheep may also have contributed to this, although this did not affect the retention of the atypical phenotype in the animal which succumbed to the oral challenge.
It is likely that it will never be possible to determine conclusively what gave rise to this change in phenotype. However, this study adds to the growing body of data which highlights a fundamental problem with prion diseases; in the absence of an agent that is structurally independent form the host genome and which can be isolated and typed, classification of natural disease relies on the phenotypic characteristics of the host. Given that some isolates appear to be unstable under certain circumstances, there is a danger in making assumptions about the disease situation in the field, and the associated public and animal health risks based on observed phenotype alone.
Supporting Information S1 File. Clinical signs of recipient animal with CH1641 scrapie. A clinical examination carried out at 514 days post inoculation reveals a bilaterally absent menace response: the sheep does not blink in response to movement of a hand/finger towards the eye but blinks when the skin surrounding the eye is touched with artery forceps. Hind limb ataxia is present (excessive swaying of the hind limbs and awkward placement of the limbs when it moves in the corner of the corridor). It bumps its head against the corner of one of the food troughs protruding into the corridor when it turns and also moves once with its head very close to the food trough after it walks from the corner towards the camera, which suggests some visual impairment. It is however able to negotiate obstacles placed on the floor of the corridor without difficulty. Camera surveillance of the pen showed abnormal lying down and rising behaviour of this sheep (identifiable by the orange arrow) compared to its pen mates (identifiable by the white circle). (MOV)
Title: Strain typing of U.S. scrapie strains using a panel of inbred mice
Author item Greenlee, Justin item Kunkle, Robert item Nicholson, Eric item Hamir, Amirali item Bulgin, Marie item Richt, Juergen Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: 7/15/2008 Publication Date: 11/15/2009 Citation: Greenlee, J.J., Kunkle, R.A., Nicholson, E.M., Hamir, A.N., Bulgin, M.S., Richt, J. 2009.
Strain Typing of U.S. Scrapie Strains Using a Panel of Inbred Mice [abstract].
American College of Veterinary Pathologists. Paper No. 121. p. 762.
Interpretive Summary:
Technical Abstract:
Prion strains may vary in their ability to transmit to humans and animals. Few experimental studies have been done to provide evidence of differences between U.S. strains of scrapie, which can be distinguished by incubation times in inbred mice, microscopic lesions, immunoreactivity to various antibodies, or molecular profile (electrophoretic mobility and glycoform ratio). Recent work on two U.S. isolates of sheep scrapie supports that at least two distinct strains exist based on differences in incubation time and genotype of sheep affected. One isolate (No. 13-7) inoculated intracerebrally caused scrapie in sheep AA at codon 136 (AA136) and QQ at codon 171 (QQ171) of the prion protein in an average of 19 months post-inoculation (PI) whereas a second isolate (No. x124) caused disease in less than 12 months after oral inoculation in AV136/QQ171 sheep. Striking differences were evident when further strain analysis was done in R111, VM, C57Bl6, and C57Bl6xVM (F1) mice. No. 13-7 did not induce disease in any mouse strain at any time post-inoculation (PI) nor were brain tissues positive by western blot (WB). Positive WB results were obtained from mice inoculated with isolate No. x124 starting at day 380 PI. Incubation times averaged 508, 559, 601, and 633 days PI for RIII, C57Bl6, VM, and F1 mice, respectively. Further passage will be required to characterize these scrapie strains in mice. This work provides evidence that multiple scrapie strains exist in U.S. sheep.
Molecular Behaviors of “CH1641-Like” Sheep Scrapie Isolates in Ovine Transgenic Mice (TgOvPrP4)▿
One of these isolates (TR316211) behaved like the CH1641 isolate, with PrPres features in mice similar to those in the sheep brain. From two other isolates (O100 and O104), two distinct PrPres phenotypes were identified in mouse brains, with either high (h-type) or low (l-type) apparent molecular masses of unglycosylated PrPres, the latter being similar to that observed with CH1641, TR316211, or BSE. Both phenotypes could be found in variable proportions in the brains of the individual mice. In contrast with BSE, l-type PrPres from "CH1641-like" isolates showed lower levels of diglycosylated PrPres. From one of these cases (O104), a second passage in mice was performed for two mice with distinct PrPres profiles. This showed a partial selection of the l-type phenotype in mice infected with a mouse brain with predominant l-type PrPres, and it was accompanied by a significant increase in the proportions of the diglycosylated band. These results are discussed in relation to the diversity of scrapie and BSE strains.
In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.
snip...see ;
Thursday, July 14, 2011
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
SHEEP AND BSE
PERSONAL AND CONFIDENTIAL
SHEEP AND BSE
A. The experimental transmission of BSE to sheep.
Studies have shown that the ''negative'' line NPU flock of Cheviots can be experimentally infected with BSE by intracerebral (ic) or oral challenge (the latter being equivalent to 0.5 gram of a pool of four cow brains from animals confirmed to have BSE).
RB264
BSE - TRANSMISSION STUDIES
Wednesday, January 18, 2012
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie
Journal of Neuropathology & Experimental Neurology:
February 2012 - Volume 71 - Issue 2 - p 140–147
MONDAY, MARCH 21, 2011
Sheep and Goat BSE Propagate More Efficiently than Cattle BSE in Human PrP Transgenic Mice
MONDAY, NOVEMBER 16, 2015
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission
MONDAY, NOVEMBER 20, 2017
*** What ever happened to 'LUCKY' the Wapiti cow elk thought to be immune from CWD with LL genotype MIA? ***
the tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
URINE
SUNDAY, JULY 16, 2017
*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***
FRIDAY, NOVEMBER 24, 2017
Norwegian Food Safety Authority makes changes to measures to limit the spread of disease Skrantesjuke (CWD) in deer wildlife
TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION
*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION
Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion...tss
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
MONDAY, JUNE 12, 2017
Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
CWD TO PIGS
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
WEDNESDAY, APRIL 05, 2017
*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***
cattle are highly susceptible to white-tailed deer CWD and mule deer CWD
***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.
SNIP...
price of prion poker goes up for cwd to cattle;
Monday, April 04, 2016
*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
SAWCorp CWD Test
PLEASE BE AWARE, SOME ARE PUSHING TO USE SAWCorp CWD Test TO ASSURE YOUR CERVID IS CWD FREE, SAWCorp CWD Test HAS _NOT_ BEEN APPROVED BY APHIS !!! IMPORTANT: SAWCorp CWD Test is Not APHIS Approved
USDA Animal and Plant Health Inspection Service sent this bulletin at 11/18/2016 11:43 AM EST
SAWCorp, a private company, recently issued a press release launching a new, patented live-animal blood test for the detection of chronic wasting disease (CWD) in cervids. A subsequent press release from the same company stated that the USDA is reviewing the test for use in the CWD program. USDA’s Animal and Plant Health Inspection Service (APHIS) does not recognize protein misfolding cyclic amplification (PMCA) prion blood tests as an official test for CWD, bovine spongiform encephalopathy,or scrapie. By definition, an official CWD test is, “Any test for the diagnosis of CWD approved by the Administrator and conducted in a laboratory approved by the Administrator in accordance with §55.8 of this part” (9 CFR Part 55).
The criteria necessary for approval as an official CWD test includes a standardized test protocol, data to support reproducibility, data to support suitability, and data to support the sensitivity and specificity of the test. While APHIS supports emerging technologies, no company has submitted the data needed for APHIS to evaluate the PMCA prion blood test. In addition, APHIS is aware of no peer-reviewed scientific publications that establish the efficacy of PMCA as a detection method for CWD in cervid blood. If producers elect to use a PMCA test, APHIS will consider positive results to be “suspect” cases that must be confirmed using an official CWD test. APHIS will not recognize negative or “not detected” PMCA test results for herd certification or interstate movement purposes.
Subject: cwd genetic susceptibility
Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§
Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g
snip...
Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.
Prion protein gene sequence and chronic wasting disease susceptibility in white-tailed deer (Odocoileus virginianus)
Adam L Brandt,1 Amy C Kelly,1 Michelle L Green,1,2 Paul Shelton,3 Jan Novakofski,2,* and Nohra E Mateus-Pinilla1,2 Author information ► Article notes ► Copyright and License information ►
The sequence of the prion protein gene (PRNP) affects susceptibility to spongiform encephalopathies, or prion diseases in many species. In white-tailed deer, both coding and non-coding single nucleotide polymorphisms have been identified in this gene that correlate to chronic wasting disease (CWD) susceptibility. Previous studies examined individual nucleotide or amino acid mutations; here we examine all nucleotide polymorphisms and their combined effects on CWD. A 626 bp region of PRNP was examined from 703 free-ranging white-tailed deer. Deer were sampled between 2002 and 2010 by hunter harvest or government culling in Illinois and Wisconsin. Fourteen variable nucleotide positions were identified (4 new and 10 previously reported). We identified 68 diplotypes comprised of 24 predicted haplotypes, with the most common diplotype occurring in 123 individuals. Diplotypes that were found exclusively among positive or negative animals were rare, each occurring in less than 1% of the deer studied. Only one haplotype (C, odds ratio 0.240) and 2 diplotypes (AC and BC, odds ratios of 0.161 and 0.108 respectively) has significant associations with CWD resistance. Each contains mutations (one synonymous nucleotide 555C/T and one nonsynonymous nucleotide 286G/A) at positions reported to be significantly associated with reduced CWD susceptibility. Results suggest that deer populations with higher frequencies of haplotype C or diplotypes AC and BC might have a reduced risk for CWD infection – while populations with lower frequencies may have higher risk for infection. Understanding the genetic basis of CWD has improved our ability to assess herd susceptibility and direct management efforts within CWD infected areas.
KEYWORDS: CWD, diplotype, G96S, PRNP, prion, synonymous polymorphism, haplotype
snip...
A solid understanding of the genetics of CWD in white-tailed deer is vital to improve management of CWD on the landscape. Most TSEs are found in domestic or captive animals where management of infected individuals is feasible. For example, scrapie infected flocks can be handled through a process generally involving genetic testing, removal and destruction of infected or suspect animals, followed by decontamination of facilities and equipment.55Containment of free ranging deer in wild populations potentially infected with CWD and decontamination of the environment is not reasonably possible. The long term effects of CWD are not yet known but it is conceivable that an unmanaged infected population would be gradually extirpated as the disease progresses56,57 or at least reduced to low densities with high disease prevalence.58,59 Either outcome would have severe ecological effects (e.g., deer play a major role in affecting plant communities60 and as a prey source61,62) as well as negative economic impacts to hunting. Overall disease prevalence has remained at relatively low levels in Illinois compared to Wisconsin.11 It is important to note that at the time of sampling, CWD had been found in 6 Illinois counties and has since been detected in 14.9Complete eradication of CWD among free ranging white-tailed deer may not be possible; however, an active containment effort in Illinois appears to have prevented significant increases in prevalence.9,11,12 Further examination of PRNP haplotype and diplotype frequencies across northern Illinois and southern Wisconsin in conjunction with population structure and movement45,63,64 will be useful in identifying localities with greater or reduced susceptibility risk. Effectiveness of CWD containment efforts can be aided through genetic testing and redirecting management resources.
***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD
In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
PRION 2016 CONFERENCE TOKYO
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
SUNDAY, DECEMBER 10, 2017
Detection of Prions in Blood of Cervids at the Asymptomatic Stage of Chronic Wasting Disease
The results showed a sensitivity of 100% in animals with very poor body condition that were IHC-positive in both brain and lymph nodes, 96% in asymptomatic deer IHC-positive in brain and lymph nodes and 53% in animals at early stages of infection that were IHC-positive only in lymph nodes. The overall mean diagnostic sensitivity was 79.3% with 100% specificity. These findings show that PMCA might be useful as a blood test for routine, live animal diagnosis of CWD.
MONDAY, SEPTEMBER 25, 2017
Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis
(ALSO, see the debate and evidence showing the origin of CWD starting in Colorado captive research pen)
Iowa Supreme Court rules law allows quarantine of CWD deer, not land
This is very, very concerning imo.
IF this ruling is upheld as such ;
''The Iowa Supreme Court upheld the district court ruling — saying the law gives the DNR only the authority to quarantine the deer — not the land. The ruling says if the Iowa Legislature wants to expand the quarantine powers as suggested by the DNR, then it is free to do so.''
IF a 'precedent' is set as such, by the Legislature not intervening to expand quarantine powers to the DNR for CWD TSE Prion, and the precedent is set as such that the cervid industry and land there from, once contaminated with the CWD TSE Prion, are free to repopulate, sell the land, etc, imo, this will blow the lid off any containment efforts of this damn disease CWD TSE Prion. The Iowa Supreme Court did not just pass the cwd buck down the road, the Supreme Court of Iowa just threw the whole state of Iowa under the bus at 100 MPH. all those healthy deer, while the litigation was going on, well, they were incubating the cwd tse prion, loading up the land even more, and in the end, 79.8% of those healthy looking deer had CWD TSE Prion. what about the exposure to the other species that come across that land, and then off to some other land? this makes no sense to me, if this is set in stone and the Legislation does not stop it, and stop if fast, any containment of the cwd tse prion will be futile, imo...terry
FRIDAY, JUNE 16, 2017
Iowa Supreme Court rules law allows quarantine of CWD deer, not land
FRIDAY, NOVEMBER 24, 2017
Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors
FRIDAY, NOVEMBER 24, 2017
Brain Tanning Hides and CWD Transmissible Spongiform Encephalopathy TSE Prion Disease Risk Factors Warning
EUROPE CWD TSE PRION
What is the risk of chronic wasting disease being introduced into Great Britain? A Qualitative Risk Assessment October 2012
Summary
Chronic wasting disease (CWD) is a highly infectious transmissible spongiform encephalopathy (TSE) that is circulating in the wild and farmed cervid populations in North America. It is the only TSE to be prevalent in free-ranging wild animal populations. A feature of CWD is its ability to spread both directly and indirectly via the contaminated environment where it is able to survive in a bio-available form for many years without any significant decrease in infectivity. Eradication of the disease from wild and farmed or managed cervid populations and the environment is extremely challenging and has not yet been successful.
Currently, there have been no reported cases of CWD or other TSE in deer in Great Britain (GB) or Europe. Given the consequences of CWD observed in North America, it is imperative that GB remains free of the disease. This risk assessment aims to assess the risk of CWD being imported into GB from North America and consequently, consider the risk of exposure and infection within the GB deer population. The assessment focuses on two main routes of entry including importation of animal feed and movement of contaminated clothing, footwear and equipment of tourists, deer hunters and British servicemen between affected areas of North America and GB. It is important to highlight that there are significant data gaps in this assessment. The main conclusions from this assessment are:
Several different animal feed products are imported into GB from North America. These include processed pet foods and consignments of unfinished feed ingredients for use in animal feed. The amount of imported feed, including pet food, that contains cervid protein is unknown and identified as a significant data gap. As non-ruminant animal feed may be produced with cervid protein (but not from positive CWD animals) in the United States (US), there is a greater than negligible risk that feed with cervid protein is imported from North America into GB. There is, however, uncertainty associated with this estimate.
In areas of North America where CWD has been reported, given that CWD is excreted in faeces, saliva, urine and blood, and survives in the environment for several years where it is able to bind to the soil, there is a medium probability that the environment (including soil) contains CWD.
Given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
Once in GB, the use of animal feed is subject to the TSE Feed Ban and ABP Regulations. In accordance with the current ban, farmed deer should not be directly exposed to (i.e. feed) imported animal feed containing any PAP. Therefore, assuming this ban is strictly adhered to, the risk of farmed and wild deer being exposed to ruminant animal feed containing deer protein from North America is considered negligible but with associated uncertainty. The probability of a (wild) deer being exposed to CWD infected deer protein in non-ruminant feed is considered to be greater than negligible but uncertain.
The pathways by which naïve deer in GB may be exposed to CWD contaminated soil and prions on equipment and clothing from people arriving in GB from North America are variable and highly uncertain. Given associated uncertainty, there is a greater than negligible probability that a person could transfer CWD prions from their contaminated equipment and/or clothing into deer habitat/environment, particularly with respect to Roe deer (Capreolus capreolus) habitat but less so for Chinese Water deer (Hydropotes inermis) habitat. Further, given the volume of tourists and other travellers moving between North America and GB, there are potentially multiple opportunities for CWD prions to be transferred from equipment to the environment.
None of the species affected by CWD in North America are present in GB. For a British species to become infected with CWD given exposure will depend on the dose and inherent susceptibility. Based on current scientific evidence Red deer (Cervus elaphus elaphus) are susceptible to CWD, Fallow deer (Dama dama) are likely to be less susceptible and Roe deer (Capreolus capreolus) have a gene conferring susceptibility. Therefore, it is likely that given exposure to an infectious dose of CWD, deer in GB could become infected with CWD.
However, given that the amount of soil ingested is likely to be very small, the probability of ingesting an infectious dose via this route is considered negligible to very low. The probability of ingesting an infectious dose via consumption of nonruminant feed is likely to be higher and may be very low, with associated uncertainty.
Overall, the probability of importing CWD into GB from North America and causing infection in British deer is uncertain but likely to be negligible to very low via movement of deer hunters, other tourists and British servicemen and very low via imported (nonruminant) animal feed. However, if it was imported and (a) deer did become infected with CWD, the consequences would be severe as eradication of the disease is impossible, it is clinically indistinguishable from BSE infection in deer (Dagleish et al., 2008) and populations of wild and farmed deer would be under threat.
What is the risk of chronic wasting disease being introduced into Great Britain? A Qualitative Risk Assessment October 2012
Thursday, April 07, 2016
What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016
Subject: DEFRA What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016
Friday, September 30, 2016
DEFRA What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016
Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT
3.5.3 Conclusions
In deer and elk, PrPCWD has a very wide and early tissue distribution, which
resembles the distribution of scrapie and BSE agents in tissues in TSE-susceptible sheep and is different to that seen in BSE in cattle. However, tissue distribution is not identical for deer4 and elk. In the latter species it accumulates later in the incubation period into detectable levels. This widespread distribution of PrPCWD early in the incubation periodpresents significant, if not insurmountable, difficulty with respect to the potential for decisions on the removal of specified risk materials (SRM) in CWD.
FRIDAY, NOVEMBER 3, 2017
BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW
''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''
IN CONFIDENCE
SATURDAY, NOVEMBER 4, 2017
FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006
Thursday, November 16, 2017
Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination
CHRONIC WASTING DISEASE CWD TSE PRION ZOONOTIC ZOONOSIS
PRICE OF TSE PRION POKER GOES UP!
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.
Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.
Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.
To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:
Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.
Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** WDA 2016 NEW YORK ***
We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans;and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
***check out this old document. some interesting stuff about USA and other Countries and concern for CWD TSE Prion. ...terry
Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT
P169 Low levels of classical BSE infectivity in rendered fat tissue
Dr. Christine Fast1, Dr. Markus Keller2, Dr. Ute Ziegler3, Prof. Dr. Martin Groschup4 1Friedrich-Loeffler-Institut, Greifswald, Germany, 2Friedrich-Loeffler-Institut, Greifswald, Germany, 3Friedrich-Loeffler-Institut, Greifswald, Germany, 4Friedrich-Loeffler-Institut, Greifswald, Germany
Aims: Specified Risk Materials (SRM) are the animal tissues potentially containing the highest levels of Bovine Spongiform Encephalopathy (BSE) prions; and their removal is the most important consumer protection measure against BSE. BSE infectivity in the mesentery fat is most likely associated with embedded nervous tissue. To date, it is unclear if contamination of the rendered fat could have occurred during tallow production at a slaughterhouse.
Methods: Samples were taken from five cattle originating from the German BSE pathogenesis study. Two animals were at preclinical, one at late preclinical and one animal at clinical stage of disease; one control animal was included. For all cattle, mouse bioassay results for the celiac and mesenteric ganglion complex (CMGC) were generated previously, showing either no, mild, moderate or substantial infectivity loads. Fat was rendered from CMGC samples embedded in mesentery fat by incubating for 20 minutes at 95°C, according to standard tallow production methods. Subsequently, the melted fat was 1:5 diluted in physiological saline and thoroughly vortexed. The liquid fat was cleaned by a short centrifugation at 10.000 rpm. Finally, 7-12 bovine prion protein overexpressing transgenic mice (Tgbov XV) were i.c. inoculated with 25-30 μl of the supernatant. Mice were sacrificed after 730 days or when showing clinical symptoms and mouse brains were subsequently examined by biochemical and immunohistochemical methods.
Results: Neither the control and the preclinical nor the late preclinical animals showed signs of infectivity in mouse bioassay of the fat samples after up to 730 days p.i. In contrast, low levels of infectivity were detected in the fat of the clinical animal as one mouse displayed a clear accumulation of pathological prion protein in the brain after an incubation period of 598 days p.i.
Conclusions: Our results clearly indicate the potential contamination of melted mesenteric fat by embedded nervous structures during standard tallow production. However, the BSE infectivity level was weak and detectable only in the fat rendered from one sample with documented high infectivity load in the ganglion itself (Kaatz et al. 2012). Albeit, this study is not representative as only one clinical animal was included, it provides a proof of principle. A broader examination would allow a better insight into temporal and spatial distribution pattern of BSE infectivity in rendered fat tissues of different origins.Such estimates have a critical role in qualitative and quantitative risk assessments and in providing advice on the designation and removal of certain SRM tissues.
=====
http://prion2017.org/programme/
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840 Next Section ABSTRACT
Chronic wasting disease (CWD) is a neurodegenerative prion disease of cervids. Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, human susceptibility to CWD is unknown. In ruminants, prion infectivity is found in central nervous system and lymphoid tissues, with smaller amounts in intestine and muscle. In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
http://jvi.asm.org/content/83/18/9608.full
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ ↵* These authors contributed equally to this work. ↵† Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA. ↵‡ Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. + See all authors and affiliations Science 24 Feb 2006: Vol. 311, Issue 5764, pp. 1117 DOI: 10.1126/science.1122864 Article Figures & Data Info & Metrics eLetters PDF You are currently viewing the abstract.
View Full Text
Abstract
The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
http://science.sciencemag.org/content/311/5764/1117.long
Dr. Christine Fast1, Dr. Markus Keller2, Dr. Ute Ziegler3, Prof. Dr. Martin Groschup4 1Friedrich-Loeffler-Institut, Greifswald, Germany, 2Friedrich-Loeffler-Institut, Greifswald, Germany, 3Friedrich-Loeffler-Institut, Greifswald, Germany, 4Friedrich-Loeffler-Institut, Greifswald, Germany
Aims: Specified Risk Materials (SRM) are the animal tissues potentially containing the highest levels of Bovine Spongiform Encephalopathy (BSE) prions; and their removal is the most important consumer protection measure against BSE. BSE infectivity in the mesentery fat is most likely associated with embedded nervous tissue. To date, it is unclear if contamination of the rendered fat could have occurred during tallow production at a slaughterhouse.
Methods: Samples were taken from five cattle originating from the German BSE pathogenesis study. Two animals were at preclinical, one at late preclinical and one animal at clinical stage of disease; one control animal was included. For all cattle, mouse bioassay results for the celiac and mesenteric ganglion complex (CMGC) were generated previously, showing either no, mild, moderate or substantial infectivity loads. Fat was rendered from CMGC samples embedded in mesentery fat by incubating for 20 minutes at 95°C, according to standard tallow production methods. Subsequently, the melted fat was 1:5 diluted in physiological saline and thoroughly vortexed. The liquid fat was cleaned by a short centrifugation at 10.000 rpm. Finally, 7-12 bovine prion protein overexpressing transgenic mice (Tgbov XV) were i.c. inoculated with 25-30 μl of the supernatant. Mice were sacrificed after 730 days or when showing clinical symptoms and mouse brains were subsequently examined by biochemical and immunohistochemical methods.
Results: Neither the control and the preclinical nor the late preclinical animals showed signs of infectivity in mouse bioassay of the fat samples after up to 730 days p.i. In contrast, low levels of infectivity were detected in the fat of the clinical animal as one mouse displayed a clear accumulation of pathological prion protein in the brain after an incubation period of 598 days p.i.
Conclusions: Our results clearly indicate the potential contamination of melted mesenteric fat by embedded nervous structures during standard tallow production. However, the BSE infectivity level was weak and detectable only in the fat rendered from one sample with documented high infectivity load in the ganglion itself (Kaatz et al. 2012). Albeit, this study is not representative as only one clinical animal was included, it provides a proof of principle. A broader examination would allow a better insight into temporal and spatial distribution pattern of BSE infectivity in rendered fat tissues of different origins.Such estimates have a critical role in qualitative and quantitative risk assessments and in providing advice on the designation and removal of certain SRM tissues.
=====
http://prion2017.org/programme/
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840 Next Section ABSTRACT
Chronic wasting disease (CWD) is a neurodegenerative prion disease of cervids. Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, human susceptibility to CWD is unknown. In ruminants, prion infectivity is found in central nervous system and lymphoid tissues, with smaller amounts in intestine and muscle. In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
http://jvi.asm.org/content/83/18/9608.full
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ ↵* These authors contributed equally to this work. ↵† Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, FL 33458, USA. ↵‡ Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. + See all authors and affiliations Science 24 Feb 2006: Vol. 311, Issue 5764, pp. 1117 DOI: 10.1126/science.1122864 Article Figures & Data Info & Metrics eLetters PDF You are currently viewing the abstract.
View Full Text
Abstract
The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
http://science.sciencemag.org/content/311/5764/1117.long
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
you can see more evidence here ;
*** WDA 2016 NEW YORK ***
We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.
We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Student Presentations Session 2
The species barriers and public health threat of CWD and BSE prions
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University
Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans.
On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.
***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations.
BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species.
This adaptation has consequences for surveillance of humans exposed to CWD.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
MONDAY, SEPTEMBER 25, 2017
Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosisF
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province! ...page 26.
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Volume 2: Science
4. The link between BSE and vCJD
4.29 The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. 1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD. It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people.
4.30 Estimates of the likely scale of a possible epidemic of vCJD are wide-ranging and the subject of much debate. To know the likely number of cases is very important, not least to enable preparations to be made for the care of victims, as well as to be able to draw up guidelines to reduce the risk of transmission from infected but asymptomatic people. Preliminary results of the study examining tonsil and appendix material for signs of infection were not informative in this regard and full results are awaited. A blood test that would allow the widespread screening of the population by a simple method is still being sought.
>>> MONDAY, NOVEMBER 06, 2017 <<<
*** Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque ***
''On secondary and tertiary transmissions, however, the proportion of PrPres positive animals gradually increased to almost 100%. Recent communications suggest that a similar situation might exist in other models of experimental exposure to prions involving swine32 and cattle33. ''
''Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque''
In conclusion, the range of incomplete syndromes that we observed between healthy carriers and typical vCJD indicates that multiple forms of prion variants can coexist and may emerge in different forms depending upon the conditions under which transmission occurred. This has obvious consequences for public health, and questions the uniqueness of the BSE/vCJD strain50 and our capacity to detect and prevent all infectious forms of prion disease.
SATURDAY, DECEMBER 02, 2017
Public health risks from subclinical variant CJD
2001 FDA CJD TSE Prion Singeltary Submission
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
MONDAY, OCTOBER 02, 2017
Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species
THURSDAY, AUGUST 17, 2017
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017 Singeltary et al
THURSDAY, JULY 13, 2017
TEXAS CREUTZFELDT JAKOB DISEASE CJD TSE PRION
Creutzfeldt Jakob Disease CJD TSE PRION QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html
http://cjdquestionnaire.blogspot.com/
http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html
http://cjdquestionnaire.blogspot.com/
WEDNESDAY, NOVEMBER 1, 2017
Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies
SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor:
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
TUESDAY, DECEMBER 12, 2017
Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017
TUESDAY, DECEMBER 12, 2017
Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017
TUESDAY, DECEMBER 12, 2017
SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017
DECEMBER 14, 2017, 20 YEARS POST DOD MOM HEIDENHAIN VARIANT CREUTZFELDT JAKOB DISEASE HVCJD DECEMBER 14, 1997, JUST MADE A PROMISE TO MOM, AND YOU DON'T BREAK PROMISES WITH YOUR MOM, NEVER FORGET, AND NEVER LET THEM FORGET...TERRY S. SINGELTARY SR.
posted by Terry S. Singeltary Sr. at
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